Failure of ST segment elevation to predict severity of acute myocardial infarction.

Abstract

Praecordial ST segment elevation was measured at 35 electrode positions in each of 40 patients admitted to a coronary care unit after acute transmural anterior myocardial infarction. Serial praecordial electrocardiographic maps were recorded to determine (a) the time course as well as reproducibility of measurements of ST segment alterations, and (b) the degree of correlation between the magnitude of ST segment elevation and the severity of infarction, as assessed clinically or by sequential estimations of serum creatine kinase activity. Large variations in ST segment elevation were found in different patients with a comparable degree of myocardial damage, and at intervals of as little as four hours in the same patient. These variations were greater than could be explained by technicalfactors, and were not related to apparent changes in the patients' clinical status. The patterns of release of myocardial creatine kinase showed that the time course of ST segment elevation was longer than the period of myocardial necrosis. No correlation was found between the myocardial infarct size as determined by enzyme release and the highest levels of ST segment elevation recorded. Thefindings suggest that ST segment elevation as measured by praecordial electrocardiographic mapping does not constitute a reliable index of the size or severity of myocardial infarcts in man.Though elevation of the ST segment of the electro-kinase (CK) activity or histological changes 24 cardiogram has been recognized for many years as hours later. The possibility has thus arisen that one of the classical signs of acute myocardial in-quantification of praecordial ST segment elevation farction (Eppinger and Rothberger, 1909), the by a simple non-traumatic technique in patients electrophysiological correlates of ischaemic injury might prove of value for the assessment of size and were not established until intracellular potentials severity of the initial ischaemic damage (Maroko could be recorded from the intact heart. It is now et al., 1972a; Reid, Pelides, and Shillingford, 1971; known that ischaemia following coronary artery Neilsen, 1973; Maroko, 1974), and that serial occlusion leads to an acceleration of repolarization, measurements might be used to evaluate subsequent with loss of resting membrane potential, which progress (Reid et al., 1974) or test the effectiveness results in ST segment elevation in the surface of drugs in altering the extent of ischaemic injury electrocardiogram (Samson and Scher, 1960;(Pelides et al., 1972; Maroko et al., 1973

Spatial and Nonspatial Influences on the TQ-ST Segment Deflection of Ischemia

“…LV ischemic sites were further subdivided into those overlying apical (1) and more basally (2) located portions of the ischemic region by a line (vertical dashed line) drawn from the site of the small artery occlusion to the apex of the heart. Nonischemic sites (7,8,9,10) were labeled as either "near" (7,9) for those within 2.0 cm of the boundary (curved dashed line) or "distant" (8,10) for those located further away. The position of the large artery occlusion is also illustrated.…”

“…Controversy has arisen recently, however, for despite all the time, effort, and resources invested in TQ-ST segment mapping studies, basic appreciation of the complex manner by which the TQ-ST segment deflection relates to the underlying ischemic region has been lacking. Inevitably, confusion and disagreement over the specificity and quantitative value of this electrocardiographic measure of myocardial injury was to be expected (3)(4)(5)(6)(7)(8)(9)(10)(11). Recognizing the current renewed interest in this area and the profound clinical value of being able to quantify ischemic damage, we have in this study examined in a theoretical and experimental manner some basic spatial and nonspatial factors influencing the magnitude and polarity of TQ-ST deflection during myocardial ischemia.…”

Relationship between epicardial ST-segment elevation and myocardial ischemic damage after experimental coronary artery occlusion in dogs.

“…Although somewhat higher correlation coefficients (r = -0.36 vs. r = -0.51) were obtained when the values for ST-segment elevation measured at 20 ms after the end of QRS were used, the relationship demonstrated was nevertheless of little value for a quantitative prediction of the degree of tissue damage for a given level of ST-segment deviation. The limitations of ST-segment elevation as a predictive index is also emphasized by studies in patients with acute myocardial infarction in whom no significant correlation was found between the summated peak precordial ST-segment elevation and ultimate infarct size calculated from the fractional disappearance curves of serum CPK activity (31).…”

Precordial electrocardiographic mapping. A technique to assess the efficacy of interventions designed to limit infarct size.

“…1) How does the normal variability of the course ofprecordial ST-segment elevation during acute myocardial infarction affect the method? Large, rapid fluctuations in ST segment may occur in the course of infarction in individual patients without obvious cause97, 98 and in a group of patients there is a progressive fall in the average ST-segment elevation as a function of time. The occurrence of these spontaneous changes in MST precludes generalization from changes of ST-segment elevation in a single patient.…”